Hyperaminoacidemia from Interrupted Glucagon Signaling Increases Pancreatic Acinar Cell Proliferation and Size via mTORC1 and YAP/TAZ Pathways

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By genetic and pharmacological disruption of glucagon receptor in mice and zebrafish, scientists reported that the ensuing hyperaminoacidemia promoted pancreatic acinar cell proliferation and cell hypertrophy, which could be mitigated by a low protein diet in mice.
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AbstractGraphical Abstract